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Related Experiment Videos

Paroxetine as a 5-HT neuroendocrine probe.

H Kojima1, T Terao, M Iwakawa

  • 1Department of Psychiatry, University of Occupational and Environmental Health School of Medicine, Yahatanishi-ku, Kitakyushu 807--8555, Japan.

Psychopharmacology
|February 26, 2003
PubMed
Summary

Low-dose paroxetine (20 mg) effectively increases ACTH and cortisol, suggesting its utility as a neuroendocrine challenge test. This response is likely mediated by 5-HT(2A/2C) receptors.

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Area of Science:

  • Neuroendocrinology
  • Pharmacology
  • Psychiatry

Background:

  • Selective serotonin reuptake inhibitors (SSRIs) like paroxetine influence brain serotonin.
  • Acute paroxetine administration has been reported to increase plasma cortisol levels in humans.
  • This suggests paroxetine's potential as a tool to investigate central serotonin pathways.

Purpose of the Study:

  • To establish a dose-response relationship for paroxetine's effects on neuroendocrine function.
  • To determine if a lower dose of paroxetine can elicit significant increases in plasma ACTH and cortisol.
  • To explore the role of 5-HT(2A/2C) receptors in paroxetine's neuroendocrine effects.

Main Methods:

  • A double-blind, cross-over study involving 20 subjects receiving placebo, paroxetine 20 mg, or paroxetine 40 mg.

Related Experiment Videos

  • Measurement of plasma ACTH and cortisol levels hourly for 6 hours post-administration.
  • An open-label substudy using cyproheptadine (a 5-HT(2) receptor antagonist) with paroxetine to assess receptor involvement.

    • Main Results:

    • Paroxetine significantly increased plasma ACTH and cortisol, with the 20 mg dose showing a more pronounced effect than 40 mg.
    • Nausea was significantly higher with 40 mg paroxetine compared to placebo.
    • Cyproheptadine partially blocked the ACTH and cortisol response to 20 mg paroxetine, but not to 40 mg.

    Conclusions:

    • Low-dose (20 mg) paroxetine is a more suitable neuroendocrine challenge agent than higher doses.
    • The observed endocrine responses to paroxetine are, at least in part, mediated by 5-HT(2A/2C) receptors.
    • Paroxetine's ability to probe serotonin function is confirmed, with implications for understanding SSRI mechanisms.